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Primidone (NCI-C56360)

Alias: NCI-C56360; Primidone; Primaclone;NCIC56360; Mylepsinum; Mizodin; Mysoline;NCI C56360;Resimatil;
Cat No.:V1669 Purity: ≥98%
Primidone (also known as NCI-C56360; NCIC56360; Mylepsinum; Mizodin; Primaclone;Mysoline; Resimatil), an analog ofphenobarbital,is an anticonvulsant of the barbiturate class.
Primidone (NCI-C56360)
Primidone (NCI-C56360) Chemical Structure CAS No.: 125-33-7
Product category: Sodium Channel
This product is for research use only, not for human use. We do not sell to patients.
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Other Forms of Primidone (NCI-C56360):

  • Primidone-d5 (primidone d5)
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Top Publications Citing lnvivochem Products
Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Primidone (also known as NCI-C56360; NCIC56360; Mylepsinum; Mizodin; Primaclone; Mysoline; Resimatil), an analog of phenobarbital, is an anticonvulsant of the barbiturate class. It is a structurally related to barbiturate-derivative anticonvulsants. Primidone can be metabolized to several active metabolites, including phenobarbital, p-hydroxyphenobarbital, and phenylethylmalonamide, which are also anticonvulsants.

Biological Activity I Assay Protocols (From Reference)
ln Vivo
Objectives: It is not known whether current use of the medication primidone affects brain gamma-aminobutyric acid (GABA) concentrations. This is an important potential confound in studies of the pathophysiology of essential tremor (ET), one of the most common neurological diseases. We compared GABA concentrations in the dentate nucleus in 6 ET patients taking primidone vs. 26 ET patients not taking primidone.
Methods: 1H magnetic resonance spectroscopy (MRS) was performed using a 3.0 Tesla Siemens Tim Trio scanner. The MEGA-PRESS J-editing sequence was used for GABA detection in two cerebellar volumes of interest (left and right) that included the dentate nucleus.
Results: The right dentate GABA concentration was similar in the two groups (2.21 ± 0.46 [on primidone] vs. 1.93 ± 0.39 [not on primidone], p=0.15), as was the left dentate GABA concentration (1.61 ± 0.35 [on primidone] vs. 1.67 ± 0.34 [not on primidone], p=0.72). The daily primidone dose was not associated with either right or left dentate GABA concentrations (respective p = 0.89 and 0.76).
Conclusions: We did not find a difference in dentate GABA concentrations between 6 ET cases taking daily primidone and 26 ET cases not taking primidone. Furthermore, there was no association between daily primidone dose and dentate GABA concentration. These data suggest that it is not necessary to exclude ET patients on primidone from MRS studies of dentate GABA concentration and, if assessment of these concentrations were to be developed as a biomarker for ET, primidone usage would not confound interpretation of the results.
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Oral primidone is up to 80% bioavailable with a Tmax if 2-4h. A 500mg oral dose of primidone Reaches a Cmax of 2.7±0.4µg/mL with a Tmax of 0.5-7h. Data regarding the AUC of primidone is not readily available.
Primidone is 72.9-80.6% recovered in urine.
The volume of distribution of primidone is 0.5-0.8L/kg.
Primidone is cleared at a rate of 30mL/min.
Mice were treated with a teratogenic dose of primidone (100 mg/kg) by gastric intubation at three different times during pregnancy, viz. days 6-14, days 12-14 on day 14 only. Blood samples were taken on day 14 at 1, 4, 8 and 24 hr after dosage. Primidone and its metabolites phenylethylmalondiamide (PEMA), and phenobarbitone, were assayed by GLC. There was no accumulation of the parent compound or the metabolites after repeated administration of primidone; each of the substances was cleared from the plasma within 24 hr. The rate of metabolism of primidone increased with prolonged treatment. The peak concentration of the metabolites was higher in the two multiple-dose groups than in the single dose group. The concentration of PEMA exceeded that of primidone between 3-8 hr and then began to decrease in the multiple-dose groups, a similar pattern was established for phenobarbitone also, although the concentrations were lower than those of PEMA.
The placental transfer of primidone and metabolites was investigated in 14 women treated for epilepsy with primidone (and additionally phenytoin, ethosuximide or valproate in 5 women) throughout pregnancy. Primidone, PEMA /phenylethylmalonamide/, phenobarbital, and polar metabolites (p-hydroxyphenobarbital and p-hydroxyphenobarbital glucuronide) were found in similar concentrations in maternal and cord blood at birth.
The pharmacokinetics of primidone (PRM) after oral administration of a single 500 mg dose was studied in 7 patients with acute viral hepatitis and 7 healthy control subjects. The elimination half-life and the apparent clearance of unchanged PRM in the patients were 18.0 +/- 3.1 hr and 42 +/- 14 mL/kg/hr, respectively (mean +/- SD) and did not differ significantly from the values in the controls (half-life 17.0 +/- 2.4 hr; clearance 35 +/- 8 mL/kg/hr). The metabolite phenylethylmalonamide (PEMA) was detected in the serum of all normal subjects within 2-24 hr. By contrast, serum levels of this metabolite were undetectable (less than 2 umol/L) in all but one of the patients. Serum levels of phenobarbital (PB) remained below the limit of detection (less than 2 umol/L) in all subjects. The findings indicate that accumulation of PRM with its attendant toxicity is unlikely to occur in epileptic patients who develop acute viral hepatitis, despite evidence that the metabolism of the drug is affected by this condition. The possibility of impaired conversion to PB and its implications are discussed.
Primidone is slowly absorbed after oral administration in the dog, with peak levels occurring 2-4 hours after dosing.
For more Absorption, Distribution and Excretion (Complete) data for Primidone (11 total), please visit the HSDB record page.
Metabolism / Metabolites
Primidone is metabolized to phenobarbitol and phenylethylmalonamide (PEMA). This metabolism is largely mediated by CYP2C9, CYP2C19, and CYP2E1.
Physiologically based pharmacokinetic modeling of the parent chemical primidone and its two metabolites phenobarbital and phenylethylmalonamide (PEMA) was applied to investigate the differences of primidone metabolism among humans, rats, and mice. The model simulated previously published pharmacokinetic data of the parent chemical and its metabolites in plasma and brain tissues from separate studies of the three species. Metabolism of primidone and its metabolites varied widely among a sample of three human subjects from two separate studies. Estimated primidone metabolism, as expressed by the maximal velocity Vmax, ranged from 0 to 0.24 mg/kg/min for the production of phenobarbital and from 0.003 to 0.02 mg/kg/min for the production of PEMA among three human subjects. Further model simulations indicated that rats were more efficient at producing and clearing phenobarbital and PEMA than mice. However, the overall metabolism profile of primidone and its metabolites in mice indicated that mice were at higher risk of toxicity owing to higher residence of phenobarbital in their tissues and owing to the carcinogenic potential of phenobarbital as illustrated in long-term bioassays. ...
The placental transfer of primidone and metabolites was investigated in 14 women treated for epilepsy with primidone (and additionally phenytoin, ethosuximide or valproate in 5 women) throughout pregnancy. Primidone, PEMA /phenylethylmalonamide/, phenobarbital, and polar metabolites (p-hydroxyphenobarbital and p-hydroxyphenobarbital glucuronide) were found in similar concentrations in maternal and cord blood at birth.
The pharmacokinetics and metabolism of primidone at steady-state were studied in 10 elderly patients aged 70-81 years and eight control subjects aged 18-26 years. Primidone half-lives and clearance values (mean +/- s.d.) were similar in the elderly and in the young (12.1 +/- 4.6 vs 14.7 +/- 3.5 hr and 34.8 +/- 9.0 vs 33.2 +/- 7.2 mL/kg/hr respectively. The serum concentrations of the metabolites phenylethylmalonamide (PEMA) and phenobarbitone relative to those of parent drug were higher in the elderly than in the young, the difference being significant (P less than 0.01) in the case of PEMA. The renal clearances of primidone, phenobarbitone and PEMA were moderately decreased in the elderly but this reduction was statistically significant only for PEMA. Elderly patients excreted a reduced proportion of unchanged primidone and an increased proportion of PEMA in urine. Ageing is associated with a greater accumulation of PEMA, which is unlikely to have a major clinical significance.
Although phenobarbital was not detected after administration of single doses of primidone, long-term administration of primidone (at various doses) in 46 epilepsy patients showed serum accumulation of phenobarbital, and PEMA /phenylethylmalonamide/. Although there was significant inter-individual variability, concentrations of the two metabolites showed correlation with those of the parent drug, and concentrations of phenobarbital were consistently higher than those of PEMA. Two of the subjects had been on a daily dose of primidone (750 mg in divided doses) for more than 3 years. After a single dose of 750 mg in this study, peak serum concentrations of primidone were achieved rapidly (by 0.5 hour), and declined slowly (half-lives, 5.3 and 7.0 hours). In both subjects, peak concentrations of metabolites, PEMA (12 and 10 ug/mL) and phenobarbital (33 and 11 ug/mL), remained relatively constant. In the cerebrospinal fluid, binding to protein by PEMA and by primidone was negligible, and approximately 60% by phenobarbital.
For more Metabolism/Metabolites (Complete) data for Primidone (9 total), please visit the HSDB record page.
Biological Half-Life
The half life of primidone is 7-22h in adults, 5-11h in children, and 8-80h in newborns.
The pharmacokinetics and metabolism of primidone at steady-state were studied in 10 elderly patients aged 70-81 years and eight control subjects aged 18-26 years. Primidone half-lives and clearance values (mean +/- s.d.) were similar in the elderly and in the young (12.1 +/- 4.6 vs 14.7 +/- 3.5 hr and 34.8 +/- 9.0 vs 33.2 +/- 7.2 mL/kg/hr respectively. ...
In a ... study in eight epileptic patients (aged 18-26 years) receiving long-term treatment with primidone (mean daily dose, 422 +/- 115 mg per day), the half-life for primidone was 14.7 +/- 3.5 hours.
The pharmacokinetics of primidone (PRM) after oral administration of a single 500 mg dose was studied in 7 patients with acute viral hepatitis and 7 healthy control subjects. The elimination half-life and the apparent clearance of unchanged PRM in the patients were 18.0 +/- 3.1 hr and 42 +/- 14 mL/kg/hr, respectively (mean +/- SD) and did not differ significantly from the values in the controls (half-life 17.0 +/- 2.4 hr; clearance 35 +/- 8 mL/kg/hr). ...
Serum half lives of primidone, PEMA /phenylethamalonamide/, and phenobarbital have been reported to be 1.85 hr, 7.1 hr, and 41 hr, respectively.
For more Biological Half-Life (Complete) data for Primidone (6 total), please visit the HSDB record page.
Toxicity/Toxicokinetics
Hepatotoxicity
In clinical trials in epilepsy, therapy with primidone was not associated with an increased frequency of serum aminotransferase elevations or liver toxicity. Primidone therapy can lead to increases in gamma glutamyltranspeptidase (GGT) levels. Elevations in alkaline phosphatase levels were largely due to bone isoforms of the enzyme. There have been no convincing reports of hepatotoxicity due to primidone in humans and no reports of its association with acute liver failure. Interestingly, primidone appears to cause cirrhosis in dogs. Because of its similarity in structure to phenytoin and phenobarbital (aromatic anticonvulsant), it has been suspected to cross react with those agents in causing anticonvulsant hypersensitivity syndrome, but convincing case reports have not been published.
Likelihood score: E* (unproven but suspected rare cause of clinically apparent liver injury).
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Ample evidence exists that primidone taken during nursing can affect the breastfed infant. Infant serum levels of primidone and its metabolites are often near or in the therapeutic range and symptoms of sedation and poor nursing have been reported. On the other hand, infants exposed in utero sometimes have withdrawal symptoms that are either alleviated by breastfeeding or worsened when breastfeeding is abruptly stopped. If the mother requires primidone, it is not a reason to discontinue breastfeeding. However, the infant must be monitored for sedation, poor feeding, poor weight gain., and developmental milestones, especially in younger, exclusively breastfed infants and when using combinations of anticonvulsant drugs. Measurement of an infant serum level might help rule out toxicity if there is a concern.
◉ Effects in Breastfed Infants
An infant death occurred from overlying and suffocation by a parent during sleep. Sedation from primidone, phenobarbital and phenytoin in breastmilk was possibly a contributing factor. Phenobarbital was found in the infant's serum (8 mg/L) and liver (16 mcg/gram) on autopsy.
A mother with epilepsy was taking primidone 250 mg 3 times daily and valproic acid 2.4 g daily during pregnancy and postpartum. During the second week postpartum, her breastfed infant was sedated. Breastfeeding was stopped and the drowsiness cleared. The sedation was possibly caused by primidone in breastmilk.
A woman taking primidone 1 gram daily and carbamazepine 1 gram daily during pregnancy and postpartum breastfed her infant for 5 weeks and noted no difference in the infant's activity before and after nursing.
A probable case of drug-induced drowsiness occurred in a newborn whose mother was taking primidone, carbamazepine and phenytoin (dosages not stated). At day 30, breastfeeding was discontinued because of the drowsiness that occurred after each feeding and poor weight gain. These authors also found that 15 partially breastfed infants whose mothers were taking anticonvulsants, including primidone, gained weight at a slower rate during the first 5 days postpartum than did 75 infants of epileptic mothers who bottle fed or control mothers taking no medications.
Possible drug-related drowsiness, pallor and feeding difficulties were reported in a 4-day-old whose mother was taking primidone 625 mg, phenobarbital 100 mg, phenytoin 200 mg and sulthiame 200 mg daily during pregnancy and postpartum. Nasogastric feeding was required for 5 weeks, during with time the infant continued to be partially breastfed.
In a cohort study of women who were taking primidone during pregnancy and their infants, 7 infants had withdrawal symptoms after birth. Of these infants, one was partially breastfed and the rest were not breastfed. In contrast, five infants who were breastfed did not have withdrawal symptoms.
Sedation lasting 5 weeks after birth and a lack of weight gain for 4 weeks after birth were reported in the exclusively breastfed infant of a mother who was taking primidone 11.4 mg/kg daily, valproic acid 13.6 mg/kg daily, and ethosuximide 11.4 mg/kg daily during pregnancy and postpartum. The reaction was possibly caused by primidone in breastmilk.
A mother with epilepsy was taking primidone 250 mg twice daily and nursing her infant. When her dose was doubled to 500 mg twice daily, a decrease in nursing was attributed to the drug in breastmilk.
A breastfed infant whose mother was taking primidone 375 mg, phenobarbital 90 mg, and carbamazepine 800 mg daily did well despite a saliva phenobarbital level of 3.4 mg/L. At 7 months of age, after the mother abruptly stop nursing, the infant had a number of "startle reactions" and infantile seizures occurred which were confirmed by an abnormal electroencephalogram. Continued phenobarbital administration to the infant for 15 months controlled the seizures and no more occurred up to 5 years of age.
A woman with long-standing seizure disorder was taking primidone and levetiracetam became pregnant. The dosage of her medications were reduced during pregnancy to provide a primidone (phenobarbital) serum concentration of 3.4 mg/L and a levetiracetam serum concentration of 40.5 mg/L. The mother was instructed to discontinue breastfeeding after 3 days. The following day her infant developed withdrawal seizures. After reinstituting breastfeeding, the infant's seizures stopped and did not recur. The infant had no abnormal findings and was thriving and seizure free at 6 months of age.
◉ Effects on Lactation and Breastmilk
No direct effect is known, but mothers taking antiepileptic drugs stop breastfeeding earlier and supplement more than mothers not taking antiepileptic drugs. Most of these reports occurred in older studies in which sedating agents such as phenobarbital and primidone were used. Infant sucking difficulties and sedation were reasons given for the reduced nursing.
Protein Binding
Primidone is 10.78-13.70% protein bound in serum.
References
Clin Neuropharmacol.2016Jan-Feb;39(1):24-8; Wikipedia.
Additional Infomation
Primidone can cause cancer according to The National Toxicology Program.
Primaclone is an odorless white crystalline powder. Slightly bitter taste. No acidic properties. (NTP, 1992)
Primidone is a pyrimidone that is dihydropyrimidine-4,6(1H,5H)-dione substituted by an ethyl and a phenyl group at position 5. It is used as an anticonvulsant for treatment of various types of seizures. It has a role as an environmental contaminant, a xenobiotic and an anticonvulsant.
Primidone is an anticonvulsant used to treat essential tremor as well as grand mal, psychomotor, and focal epileptic seizures. Primidone was developed by J Yule Bogue and H C Carrington in 1949. Primidone was granted FDA Approval on 8 March 1954.
Primidone is an Anti-epileptic Agent. The physiologic effect of primidone is by means of Decreased Central Nervous System Disorganized Electrical Activity.
Primidone is an aromatic anticonvulsant used to treat complex, partial and generalized seizures. Therapy with primidone can be associated with increases in gamma glutamyltranspeptidase levels, but is not associated with serum aminotransferase elevations, and despite its similarity in structure to phenobarbital and phenytoin, clinically apparent liver injury from primidone has not been reported and must be quite rare if it occurs at all.
Primidone is an analog of phenobarbital with antiepileptic property. Although the mechanism of action has not been fully elucidated, primidone probably exerts its actions, in a manner similar to phenobarbital, via activation of gamma-aminobutyric acid (GABA)-A receptor/chloride ionophore complex, which leads to prolonged and increased frequency of opening of the chloride channel within the receptor complex. This results in an alteration in the electrical activity of the nerve cell membrane, causing hyperpolarization and prevention of partial and tonic-clonic seizures. In addition, this agent is partially metabolized to phenobarbital and phenylethylmalonamide (PEMA), which may also contribute to its anti-seizure properties.
A barbiturate derivative that acts as a GABA modulator and anti-epileptic agent. It is partly metabolized to PHENOBARBITAL in the body and owes some of its actions to this metabolite.
Drug Indication
Primidone is commonly indicated for the management of grand mal, psychomotor, and focal epileptic seizures. In addition, it has also been studied and utilized as an effective management of essential tremor.
FDA Label
Mechanism of Action
Primidone and its metabolites, phenobarbital and phenylethylmalonamide (PEMA), are active anticonvulsants. Primidone does not directly interact with GABA-A receptors or chloride channels but phenobarbital does. Primidone alters transmembrane sodium and calcium channel transport, reducing the frequency of nerve firing, which may be responsible for the primidone’s effect on convulsions and essential tremor.
The melastatin-related transient receptor potential (TRP) channel TRPM3 is a nonselective cation channel expressed in nociceptive neurons and activated by heat. Because TRPM3-deficient mice show inflammatory thermal hyperalgesia, pharmacological inhibition of TRPM3 may exert antinociceptive properties. Fluorometric Ca influx assays and a compound library containing approved or clinically tested drugs were used to identify TRPM3 inhibitors. Biophysical properties of channel inhibition were assessed using electrophysiological methods. The nonsteroidal anti-inflammatory drug diclofenac, the tetracyclic antidepressant maprotiline, and the anticonvulsant primidone were identified as highly efficient TRPM3 blockers with half-maximal inhibition at 0.6 to 6 uM and marked specificity for TRPM3. Most prominently, primidone was biologically active to suppress TRPM3 activation by pregnenolone sulfate (PregS) and heat at concentrations markedly lower than plasma concentrations commonly used in antiepileptic therapy. Primidone blocked PregS-induced Cai influx through TRPM3 by allosteric modulation and reversibly inhibited atypical inwardly rectifying TRPM3 currents induced by coapplication of PregS and clotrimazole. In vivo, analgesic effects of low doses of primidone were demonstrated in mice, applying PregS- and heat-induced pain models, including inflammatory hyperalgesia. Thus, applying the approved drug at concentrations that are lower than those needed to induce anticonvulsive effects offers a shortcut for studying physiological and pathophysiological roles of TRPM3 in vivo.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C12H14N2O2
Molecular Weight
218.25
Exact Mass
218.106
CAS #
125-33-7
Related CAS #
Primidone-d5;73738-06-4
PubChem CID
4909
Appearance
White to off-white solid powder
Density
1.138g/cm3
Boiling Point
520.7ºC at 760mmHg
Melting Point
281-282°C
Flash Point
228.2ºC
Vapour Pressure
6.08E-11mmHg at 25°C
Index of Refraction
1.528
LogP
1.195
Hydrogen Bond Donor Count
2
Hydrogen Bond Acceptor Count
2
Rotatable Bond Count
2
Heavy Atom Count
16
Complexity
279
Defined Atom Stereocenter Count
0
InChi Key
DQMZLTXERSFNPB-UHFFFAOYSA-N
InChi Code
InChI=1S/C12H14N2O2/c1-2-12(9-6-4-3-5-7-9)10(15)13-8-14-11(12)16/h3-7H,2,8H2,1H3,(H,13,15)(H,14,16)
Chemical Name
5-ethyl-5-phenyl-1,3-diazinane-4,6-dione
Synonyms
NCI-C56360; Primidone; Primaclone;NCIC56360; Mylepsinum; Mizodin; Mysoline;NCI C56360;Resimatil;
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO:44 mg/mL (201.6 mM)
Water:<1 mg/mL
Ethanol:3 mg/mL (13.7 mM)
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (11.45 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.5 mg/mL (11.45 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (11.45 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.


 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 4.5819 mL 22.9095 mL 45.8190 mL
5 mM 0.9164 mL 4.5819 mL 9.1638 mL
10 mM 0.4582 mL 2.2910 mL 4.5819 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Method for preparing DMSO stock solution mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.

Method for preparing in vivo formulation:Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.

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